Saturday, June 30, 2012

Large electrical storms on the east coast disrupted power for
Amazon.com Inc. cloud-computing operations Friday night, causing outages
for customers such as Netflix Inc. and photo-sharing service Instagram.

The Seattle-based online retailer operates data centers with servers
that manage the Web operations of many other companies, a practice often
called cloud computing. Power outages caused by catastrophic storms
that blanketed the east coast affected Amazon's operations in Virginia.

On Saturday afternoon, Amazon was still reporting performance issues
for what it calls its elastic cloud compute, relational database and
elastic beanstalk services. The problems appeared to have begun
appearing on the site at around 11:21 p.m. EDT on Friday.

For those old guys like me who had built global networks on their own nickle, this was always a risky business. There was just a storm, guys, not an asteroid. You should have planned for that. Secon exits, Plan B, whatever! I have seen them all...

Prior planning prevents poor performance ... my father always said that to me!

Friday, June 29, 2012

To an economist, perhaps, there is no difference between activity and inactivity; both have measurable economic effects on commerce. But the distinction between doing something and doing nothing would not have been lost on the Framers, who were “practical statesmen,” not metaphysical philosophers.

Thursday, June 28, 2012

In the two years since the AHCA passed, My family has saved over
2000.00. My son, 24 has remained on my policy (I had been paying 400 a
month for his insurance as he began his career.) My mother's drug bill
dropped by several hundred dollars.

Now I can feel comfortable that my children, both who have had earlier
bouts with respiratory illness but seem fine now, will not have to be
saddled with high premiums or exclusions for pre-existing conditions.

I can feel comfortable that people I come into contact with who haven't had insurance will now be able to afford it.

Perhaps this reader will tell me who is paying for this? They are apparently clueless on this issue. Health Care is not free, that is the point. When some person makes a comment like this it is clear to me that they have not a single idea that there are consequences. Even in Aristotle's day we knew every action had a reaction, in fact for 2,000 years that was the basis of the theories of motion, not some force at a distance. Somehow or other this people have a Newtonian idea that there is some force field of zero costs that enables all of this.

Every comment the above makes has a consequence, a cost, and yet the writer is totally above reality in never recognizing them.

At the other extreme as I had said some 3+ years ago as this disaster was brewing, Government mandates must carries, services few use and many abuse, and we all pay. A sad day for America, few of us ever understand the costs side, too many live in the wonderland of Government gifts.

I have always had mixed feelings about Rousseau. Today marks the 300th anniversary of his birth. I remeber spending quite a bit of time in Annecy on the lake in Savoy, visiting his old haunts.

Here was a man who thought we humans perfect until destroyed by society and a man who believed truly in the ideal of a social contract. He was a man also estranged from time to time from his peers but a man held up by many. In ways a counterpart of Voltaire and yet distant from him as well.

His works may seem strange to many Americans today but to the "intellectuals" of the mid 18th century they caused bells to ring.

Consider his words:

The most ancient of all societies, and the only one that is natural, is the
family: and even so the children remain attached to the father only so
long as they need him for their preservation. As soon as this need
ceases, the natural bond is dissolved. The children, released from the
obedience they owed to the father, and the father, released from the
care he owed his children, return equally to independence. If they
remain united, they continue so no longer naturally, but voluntarily;
and the family itself is then maintained only by convention.

Strange is it not for he was the one who abandoned his own children. But read deeper, does he justify this action, is it not now a natural progression?

After these 300 years, one should at least reflect briefly on what this man meant to us today. On the one hand the Progressives and their view of a social contract, on the other, the Individualists and their ideal of the independence of man.

Wednesday, June 27, 2012

Signaling pathways in the cells have been a major focus on study for the past decade or so. The focus generally has been on what protein or gene influences what other protein or gene. A recent article in Science presents some interesting work on Wnt and TERT.

Wnt is an extra cellular signaling protein and it attaches to Frizlled a receptor and sets off a cascade that moves B catenin into the nucleus and generates Myc which is a transcription protein with together with catenin and other transcription proteins generates Tert from TERT.

Telomerase is a ribonucleoprotein polymerase that maintains telomere
ends by addition of the telomere repeat TTAGGG. The enzyme consists of a
protein component with reverse transcriptase activity, encoded by this
gene, and an RNA component which serves as a template for the telomere
repeat. Telomerase expression plays a role in cellular senescence, as it
is normally repressed in postnatal somatic cells resulting in
progressive shortening of telomeres. Deregulation of telomerase
expression in somatic cells may be involved in oncogenesis.

As the Science article states:

Maintaining the length of telomere, the ends of chromosomes, is essential for all cells that divide many times. The enzyme telomerase lengthens these ends, counterbalancing their shortening that occurs each time chromosomes are copied. Telomerase is essential for cell viability, and loss of its function from the loss of only one of two copies of the encoding gene can lead to the failure of stem cell renewal that is seen in premature aging conditions such as dyskeratosis congenita, aplastic anemia, and pulmonary fibrosis. Conversely, telomerase activity is increased in many cancers and may be required for cancer cells to maintain their telomere length...

They continue is a rather interesting wording:

Because of the importance of telomerase expression, the signaling pathways that control TERT transcription have been extensively studied. Remarkably, many different transcription factors, including c-Myc, Sp1, nuclear factor of activated T cells (NFAT), activating protein 2B, nuclear factor κB (NF-κB), Myb, activating transcription factor, nuclear factor 1 (NF1), and the estrogen receptor (ER), bind to the 330–base pair minimal TERT promoter and regulate transcription. In addition, a number of negative regulators bind the TERT promoter, including CTCF, elongation factor 2, p53, Ets, Mad1, Men1, and Wt1. Adding β-catenin and Klf4 to the many regulators that bind the TERT promoter is like adding one more guest to a crowded table at a dinner party.

They conclude:

It is reasonable to propose that Wnt regulates TERT given that Wnt signaling plays an essential role in stem cell self-renewal and that TERT is needed for the long-term growth of stem cells. TERT regulation seems to require not one, but two master transcriptional regulators to assure that there is neither too much, which may allow the growth of cancer cells, nor too little, which might lead to stem cell failure. The fi nding by Hoffmeyer et al. that both β-catenin and Klf4 are required to activate TERT expression puts the horse (Wnt) before the cart (TERT) and provides a foundation for linking telomerase levels and self-renewal.

The observation of the inter-cellular signalling with Wnt and its control over TERT and the telomere process is quite interesting. This may be an interesting way to incorporate many of the Turing models we have been discussing as well.

The NY Times has an article regarding the intent by cable companies to charge for usage. The state:

Here in South Texas, Time Warner Cable
customers have been given the online equivalent of a scale in the
bathroom, a “usage tracker” that adds up all the household’s Facebooking
and YouTubing. Customers who sign up for a light plan of 5 gigabytes of
broadband — that’s the equivalent of two high-definition movie
downloads — are rewarded with a $5 discount each month if they don’t go
over. If they do, they pay $1 for every additional gigabyte.

then continue:

Usage-based billing is seen by some as a fairer alternative to broadband
caps, a term most closely associated with Comcast, which had been
enforcing a limit of 250 gigabytes per Internet customer per month.
Although only a small minority of customers ever exceeded the cap, it
became a lightning rod for competitors like Netflix, which accused
Comcast of unfairly favoring its own services.

Now a bit of bona fides. I was COO of NYNEX Mobile, now Verizon, and SVP at Warner Cable, then Warner AMEX. I thus have some modicum of knowledge. Also as the CEO and founder of central and eastern Europe's first full fiber network I understand Internet backbone. Unlike many of the younger generation I went thru these wars before.

My observations:

1. Billing is a total nightmare. Really. It costs more than anything you hope to recover. Really. Been there done that! Why? Because customers complain and seek remedies for calls not made, bytes not used. You have to be a complete moron, I will tell you how I really feel later, to think you will win this one. Average work here. Yes, some people use nothing, lots frankly, you win, a few are hogs, you lose. So figure out what works and you will never get a complaint, or a law suit!

2. What is the cost? Zero now, almost. It does not cost much anymore, even if you are not a Tier 1 Internet backbone carrier, which all of these guys are any how. Are you just greedy?

3. The real and only reason is to establish a barrier to entry to competitors. Yes, the cable guys want to control content, that is where the money is. This is their way to do that. It is a pre-emptive strike. Perhaps there are still anti-trust laws, like bundling and the like.

The Times missed the point. The FCC is clueless on this as is Justice. It must become a total mess before anyone acts. Just watch.

Tuesday, June 26, 2012

I have difficulty in decoding the usage of names. Let me give several examples:

1. When back in a hospital I get called Dr. McGarty no matter what, even though I am not licensed to practice Medicine. A couple of years ago when back at the Brigham this was pandemic. For a while I thought I was in a 1950s movie of Dr Kildare.

2. In a medical specialists office I am called Dr. McGarty by the staff and depending on how well I know the specialist it is Terry or Dr McGarty.

3. In upscale professional settings such as a good law firm it is Mr. McGarty.

4. By anyone under 40 it is Terrence if they have no clue who I am. Now I never use Terrence other than in a legal context, for after all it is my first name.

5. In my local doc's office, nice local guy, his staff calls me Terrence. As if I and all the other patients were pets, Spotty, Rover, etc. I remember my first copy of Harrison's I think the 5th edition, used, the first chapter was on how to greet patients. "Mr Jones" or "Mrs Smith", well before Gloria Steinham. One demonstrated respect, and perhaps a professional approach.

6. At a trial if one wants to denigrate a witness one calls them by their first name. Old trick.

7. But what has happened to the younger set? Answer, teachers. They were the one's who established the code of human interaction, and well they went down the drain. In an academic setting it was and may still be at better institutions Prof. McGarty etc. Yet at low level institutions, such as my local Community College, it was Terrence.

So what is in a name? It tells you the "class" of the user. Yes, class, it is like the use of "huh" or "uh" or "Um". Animal grunts, resulting from the collapse of our primary and secondary educations system. Do we have problems, yes indeed, and it begins with manners.

Saturday, June 23, 2012

The NY Times has a piece commemorating Turing's 100th birthday anniversary today. Despite Turing's work on computers and codes, in the long run it may be one of his last papers published in August 1952, entitled (he died June 7, 1954):

The Chemical Basis of Morphogenesis, Phil Trans Royal Society London pp 37‐72, 1952

He states in the Abstract:

It is suggested that a system of chemical substances, called morphogens, reacting together and diffusing through a tissue, is adequate to account for the main phenomena of morphogenesis. Such a system, although it may originally be quite homogeneous, may later develop a pattern or structure due to an instability of the homogeneous equilibrium, which is triggered off by random disturbances. Such reaction-diffusion systems are considered in some detail in the case of an isolated ring of cells, a mathematically convenient, though biologically unusual system.

The investigation is chiefly concerned with the onset of instability. It is found that there are six essentially different forms which this may take. In the most interesting form stationary waves appear on the ring. It is suggested that this might account, for instance, for the tentacle patterns on Hydra and or whorled leaves. A system of reactions and diffusion on a sphere is also considered. Such a system appears to account for gastrulation. Another reaction system in two dimensions gives rise to patterns reminiscent of dappling. It is also suggested that stationary waves in two dimensions could account for the phenomena of phyllotaxis.

The purpose of this paper is to discuss a possible mechanism by which the genes of a zygote may determine the anatomical structure of the resulting organism. The theory does not make any new hypotheses; it merely suggests that certain well-known physical laws are sufficient to account for many of the facts. The full understanding of the paper requires a good knowledge of mathematics, some biology, and some elementary chemistry. Since readers cannot be expected to be experts in all of these subjects, a number of elementary facts are explained, which can be found in text-books, but whose omission would make the paper difficult reading.

Frankly the paper has lasting insight which may surface again as we examine metastatic processes and intra/extra cellular signalling.

It should be noted that the pattern in the above Hemerocallis can be explained by Turing's work. For those who understand the wave equation with a nonlinear constraint then we see two waves of red, one in the center and one at the edge (see my paper on Turing coloring). It can likewise be argued that the flow of inter-cellular ligands in metastatic cancers follow a similar model (see my White Paper).

One can only imagine what would have happened if he had gotten further with the Watson and Crick paper, dated April 25, 1953.

Friday, June 22, 2012

LKB1 has been demonstrated to be the underlying control
element in Peutz-Jeghers syndrome, a proliferative melanocytic genetically
dominant disorder. It controls certain pathways and as a result can be
considered as a candidate in the development and progression of melanoma.
Generally LKB1 is a gene whose protein stabilizes the growth and location of
melanocytes. Understanding its impact in Peutz-Jeghers allows one to examine
what happens when its function is suppressed in melanoma. Albeit not an
initiator in the process, its aberration in a melanocyte argues for movement
and loss of control.

In a recent paper by Liu et al the authors examine this
premise and conclude that loss of LKB1 is significant especially in metastatic
evolution. As Liu et al state:

Germline mutations in LKB1 (STK11) are associated with
the Peutz-Jeghers syndrome (PJS), which includes aberrant mucocutaneous
pigmentation, and somatic LKB1 mutations occur in 10% of cutaneous melanoma. By
somatically inactivating Lkb1 with K-Ras activation (±p53 loss) in murine
melanocytes, we observed variably pigmented and highly metastatic melanoma with
100% penetrance. LKB1 deficiency resulted in increased phosphorylation of the
SRC family kinase (SFK) YES, increased expression of WNT target genes, and
expansion of a CD24+ cell population, which showed increased
metastatic behavior in vitro and in vivo relative to isogenic CD24−
cells. These results suggest that LKB1 inactivation in the context of RAS
activation facilitates metastasis by inducing an SFK-dependent expansion of a
prometastatic, CD24+ tumor subpopulation.

Earlier work by Zheng et al noted:

The LKB1-AMPK signaling pathway serves as a critical cellular
sensor coupling energy homeostasis to cell growth, proliferation, and survival.
However, how tumor cells suppress this signaling pathway to gain growth
advantage under conditions of energy stress is largely unknown.

Here, we show that AMPK activation is suppressed in
melanoma cells with the B-RAF V600E mutation and that downregulation of B-RAF
signaling activates AMPK. We find that in these cells LKB1 is phosphorylated by
ERK and Rsk, two kinases downstream of B-RAF, and that this phosphorylation
compromises the ability of LKB1 to bind and activate AMPK. Furthermore, expression
of a phosphorylation-deficient mutant of LKB1 allows activation of AMPK and
inhibits melanoma cell proliferation and anchorage-independent cell growth.

Our findings provide a molecular linkage between the
LKB1-AMPK and the RAF-MEK-ERK pathways and suggest that suppression of LKB1 function
by B-RAF V600E plays an important role in B-RAF V600E-driven tumorigenesis.

Thus Zheng et al putatively identified these two pathways as
sources for melanoma development. Liu et al appear to have extended this to
metastasis.

Now in a paper by Bauer and Stratakis the authors provide an
excellent overview of the controlling pathways. We provide a revised version of
their pathway controls in a normal melanocyte below.

The LKB1 gene, also called STK11, which encodes a member of
the serine/threonine kinase, regulates cell polarity and functions as a tumour
suppressor. This is clearly demonstrated in the above.

Now Liu et al state regarding this pathway model:

Two independent pathways appear to be critically
important in regulating cell growth in response to nutrient supply and
mitogenic stimulation:

Recent evidence suggests that the tumour suppressor gene
complex, TSC1/TSC2, orchestrates the signal from both pathways to the
downstream target, mTOR, which in turn regulates the ribosomal protein S6 and
4EBP-1, a repressor of the translational initiation factor eIF4E. In this
model, at times of nutrient stress LKB1/AMPK activation of the TSC1/TSC2
complex results in inhibition of mTOR and a decrease in protein synthesis.
Under stimulation of mitogenic pathways, PI3K phosphorylates PIP2 to PIP3
resulting in recruitment of AKT to the membrane where it is activated by PDK1.
Activated AKT inhibits the TSC1/TSC2 tumour suppressor complex leading to
increased mTOR activity. In the later pathway, PTEN antagonises PIP3 action
through dephosphorylation, and thus provides an ‘‘off’’ switch for regulating
mitogenic pathway induced cellular growth and proliferation.

Cross talk of several other pathways appears to play
important regulatory roles in the lentiginoses syndromes to include the
Ras/MAPK pathway in the regulation of translation, the LKB1 pathway in cellular
polarity, the AKT pathway (as well as the TSC1/TSC2 complex) in the regulation
of the Wnt/GSK3b/b-Cat pathway, and the BMP pathway in the regulation of PTEN
(see text for further discussion). Lastly, both PTEN and mTOR appear to have
negative regulatory effects on VEGF through loss of stabilisation of the
hypoxia inducible transcription factor 1 (HIF1).

When LKB1 is inactivated we have the following changes
observed:

These models or Bauer and Stratakis are compelling and
establish a paradigm which the work of Liu et al can be considered.

Let us go back to LKB1 and its function. From NLM database
we have[1]:

LKB1 is a primary upstream kinase of adenine
monophosphate-activated protein kinase (AMPK),
a necessary element in cell metabolism that is
required for maintaining energy homeostasis. It is now clear that LKB1 exerts its
growth suppressing effects by activating a group of other ~14 kinases,
comprising AMPK and AMPK-related
kinases.

Activation of AMPK by LKB1 suppresses growth
and proliferation when energy and nutrient levels are scarce. Activation of
AMPK-related kinases by LKB1 plays vital roles maintaining cell polarity
thereby inhibiting inappropriate expansion of tumour cells. A picture from
current research is emerging that loss of LKB1 leads to disorganization of cell
polarity and facilitates tumour growth under energetically unfavorable
conditions. Also it is known as PJS; LKB1; hLKB1.

This gene, which encodes a member of the serine/threonine
kinase family, regulates cell polarity and functions as a tumor suppressor.
Mutations in this gene have been associated with Peutz-Jeghers syndrome, an
autosomal dominant disorder characterized by the growth of polyps in the
gastrointestinal tract, pigmented macules on the skin and mouth, and other
neoplasms. Alternate transcriptional splice variants of this gene have been
observed but have not been thoroughly characterized.

AMP-activated protein kinase (AMPK) is a highly conserved
sensor of cellular energy status found in all eukaryotic cells. AMPK is
activated by stimuli that increase the cellular AMP/ATP ratio. Essential to
activation of AMPK is its phosphorylation at Thr-172 by an upstream kinase,
AMPKK, whose identity in mammalian cells has remained elusive.

Here we present biochemical and genetic evidence
indicating that the LKB1 serine/threonine kinase, the gene inactivated in the
Peutz-Jeghers familial cancer syndrome, is the dominant regulator of AMPK
activation in several mammalian cell types. We show that LKB1 directly
phosphorylates Thr-172 of AMPKalpha in vitro and activates its kinase activity.

LKB1-deficient murine embryonic fibroblasts show nearly
complete loss of Thr-172 phosphorylation and downstream AMPK signaling in
response to a variety of stimuli that activate AMPK. Reintroduction of WT, but
not kinase-dead, LKB1 into these cells restores AMPK activity. Furthermore, we show
that LKB1 plays a biologically significant role in this pathway, because
LKB1-deficient cells are hypersensitive to apoptosis induced by energy stress.

On the basis of these results, we propose a model to
explain the apparent paradox that LKB1 is a tumor suppressor, yet cells lacking
LKB1 are resistant to cell transformation by conventional oncogenes and are
sensitive to killing in response to agents that elevate AMP. The role of
LKB1/AMPK in the survival of a subset of genetically defined tumor cells may
provide opportunities for cancer therapeutics.

Also Shaw et al demonstrate several ways in which LKB1 can function when
activated in vivo from either a basal or non-basal state. The description can
be shown in the following Figure:

However, although this is an interesting and compelling
description of the metastatic driving factors, there are a multiple set of
issues still outstanding:

1. Metastatic behavior implies the ability of the malignant
melanocyte to migrate at will within the body. Movement of the melanocyte
requires breaking of the E cadherin bonds with the adjacent keratinocytes. Thus
is there a sequence of genetic changes and how does this putative mechanism
relate to that of the E cadherin mechanism.

As Baas et al state:

A
second prominent aspect of polarized simple epithelia is the presence of
junctional complexes at the apical boundaries between neighboring cells. These
junctions form an impenetrable seal between cells and provide strength to the
epithelial sheet by serving as anchoring sites for cytoskeletal elements
including the brush border.

We
found that LS174T cells do not express junctional proteins, such as ZO-1, and
are homozygous mutant for E-cadherin. By contrast, DLD-1 cells are capable of
forming tight junctions and adhesion junctions when grown to confluency and
appear to express most junctional compo­nents already at low-cell density.

We
determined the localization of the tight junction component ZO-1 and of the
adherens junction protein p120 before and after activation of LKB1 in DLD-1-W5
cells grown at very low density.

2. LKB1 is a gene related to the control from decreased
nutrients. However we have the angiogenesis issue related to the increased
nutrition of malignant cells. However on the counter side we have the Warburg
effect as a counter to normal metabolism, namely cancer cells are anaerobic
metabolic systems. What is the balance between the two?

3. Is the LKB1 mutation one of random gene mutations or is
it a direct consequence of other downstream mutations? Is perhaps this loss of
LKB1 a result of some induced miRNA effect in vivo?

In a recent paper by Perry et al, Stratifying Type 2
Diabetes Cases by BMI Identifies Genetic Risk Variants in LAMA1 and
Enrichment for Risk Variants in Lean Compared to Obese Cases, the authors have
performed a genome wide study identifying genes that a prevalent in non-obese
versus obese Type 2 diabetics[1] (T2). We have argued
previously that the predominant number of T2 cases is driven by obesity. The
authors demonstrate non obese T2 and then through a genome wide analysis, GWA,
identify the putative genes.

We summarize their results and we then present several
questions regarding the usefulness of the results.

The authors start by stating:

Individuals with Type 2 diabetes (T2D) can present with
variable clinical characteristics. It is well known that obesity is a major
risk factor for type 2 diabetes, yet patients can vary considerably—there are
many lean diabetes patients and many overweight people without diabetes. We
hypothesized that the genetic predisposition to the disease may be different in
lean (BMI&lt;25 Kg/m2) compared to obese cases (BMI≥30 Kg/m2).

Using these data we found differences in genetic enrichment
between lean and obese cases, supporting our original hypothesis. We also
searched for genetic variants that may be risk factors only in lean or obese
patients and found two novel gene regions not previously reported in European
individuals. These findings may influence future study design for type 2
diabetes and provide further insight into the biology of the disease.

The GWA studies of type 2 diabetes have not so far
provided a greatly improved understanding of the clinical heterogeneity of the
disease. Type 2 diabetes cases vary appreciably in their clinical
characteristics, particularly age of diagnosis and body mass index (BMI). There
is also a group of patients who may present with evidence of an autoimmune
component to their diabetes, but who are not insulin dependent. In contrast,
the identification of the genetic component to monogenic forms of diabetes has
often explained the clinical heterogeneity observed.

Previous studies have provided some evidence of genetic
heterogeneity between non-obese and obese type 2 diabetic cases. For example,
the variant with the strongest effect on type 2 diabetes risk, in TCF7L2, has a stronger effect in non-obese cases (odds
ratio = 1.53 [0.37–1.71] compared to obese cases (OR = 1.21 [1.09–1.35]). The
effect of FTO variation on type 2 diabetes risk depends on how
cases and controls are ascertained by BMI status, but this was expected given FTO's known primary effect on BMI. In the most recent
GWA studies of type 2 diabetes, risk variants tended to have stronger effects
in non-obese compared to obese individuals – of 30 loci examined, 23 showed
stronger associations in non-obese compared to obese individuals.

The authors conclude:

In conclusion, we report associations with the LAMA1 and
HMG20A
(not previously associated at genome-wide significance in Europeans)
gene regions with type 2 diabetes risk. We have demonstrated that lean diabetic
cases are enriched for known type 2 diabetes risk alleles compared to obese
cases. This enrichment is consistent with the observation that many of the
variants with the strongest effects on diabetes are associated with reduced
beta cell function [1]. At the opposite end of the spectrum, obese cases presumably
need fewer diabetes risk variants to push them towards diabetes, as they are
already under strain from the physiological impact of obesity and insulin
resistance. These data suggest a disease model where type 2 diabetes cases lie
across a continuous distribution with regards to genetic/environmental risk,
and betacell dysfunction versus insulin resistance aetiologies.

The conclusion is that lean or low BMI Pt with T2 has a
genetic predisposition to the disorder. This is consistent with what we have
been stating in our prior analyses but it fails to demonstrate what percent of
the total population has such a genetic failure.

This report raises several questions:

1. Not apparent is the percent of Type 2 patients who have
low BMI, &lt;25, and the percent who have high, >30. Namely what is the
incidence and prevalence of T2 in those groups? One would suspect based on
generally available data that the percent of high BMI individuals having T2 is
high and those with low BMI have a low percent incidence and prevalence.

2. With the genes identified in the GWA in the low BMI
group, what is their function? Namely the authors should have explored the
intra-cellular and intercellular pathways and their metabolic effects. Just
have a gene present does not mean causality. Causality is an essential element.
Presence is at best correlative.

3. There is the issue of somatic presence versus germline
presence. Namely if the Pt with low BMI and gene variants, were these somatic,
namely did they have this forever and if so why did they come down with T2 at
some point. If not somatic, and germline then what process caused the gene
mutation. What caused the gene variant? This is a key question. Also if somatic
why did it take so long to present?

4. How do we define T2? I suspect the authors do so via an
HbA1c measure. They seem to allude to such by taking measurements of HbA1c as
well as 2 hour glucose as one would do in a classic glucose tolerance test
using a 75g glucose bolus. However, I found it difficult to identify the
specific definition used in the document itself.

5. Notwithstanding, there is the annoying mass balance equation, input-output=net accumulation! How do these genes change this? Do they result in lowered metabolic expenditures? But with low BMI this is not an issue. Thus are we looking at different T2 disease states? The low BMI T2 patient has excess blood glucose due to lower uptake? lower insulin secretion? Why? What do these genes do to achieve that abnormality?

We seem left with more questions than answers. This is often the case with excess data and no paradigms to validate them.

Thursday, June 21, 2012

The New Yorker has a piece which excoriates Mrs. Romney's horse. Now I am not a big horse fan, I did clean stables in New York City, got stiffed by the owner, I believe it was in 1956, St Patrick's day to be precise. The old man owner had us clean out stables in return for payment. When all done he told us we were paid by learning how to work. This was a critical life lesson, always have a contract and never trust someone you do not know. As I later dealt with many international deals I always remembered the stiffing dealt by the old man owner, a permanent limbic valence.

I also rode a bit when in New Mexico, north of Taos, great riding, and in Virginia, all western. But I do appreciate dressage and I was personally introduced to Mrs. Romney's horse this past week.

But like any sport it does take effort, expertise, dedication. Also one should remember that Bloomberg's daughter is also in the sport.

So why the uproar, from Colbert? To those uneducated I guess it looks funny. But one should remember that sixty years ago it was dominated by the US Army! Yes soldiers were the riders and the Government frequently the owner.

You see it was the cavalry which started this and when they moved to tanks then it was moved to those who could afford it. This is not an inexpensive sport. Riders, trainers, vets, stable hands, and the list goes on. But frankly the animals are magnificent.

But the New Yorker should remember, never get between a girl and her horse.

Wednesday, June 20, 2012

Pennsylvania has some of the worst road maintenance practices in the world. Somehow they manage to take massive Interstate roads and close them to one lane on upgrades which are heavily traveled by trucks. I experienced 2-3 hour delays on I78 the other day as I observed these trucks in single file down to 20-30 mph and blockages some 6-10 miles long. The wasted fuel, time, costs, and when one passes the blockage there is no one doing anything but there is a sign proclaiming this a shovel ready stimulus job! Three years later!

Then there is New Jersey. Five lane highways, and they are expanding the NJ Turnpike an additional 3 lanes in each direction. Hundreds of people and moving machines. No delays, the trucks are doing 70+. And no Stimulus sign.

Why the difference? Is Pennsylvania that incompetent. New Jersey seems to have managed this through some of the most incompetent Governors, and we have had quite a few. Why the difference?

I get the impression that many Americans believe Medicare is financed
like Social Security. They know that a portion of payroll taxes goes to
Social Security and a portion goes to Medicare. So they conclude
workers are paying for Medicare benefits the same way they are paying
for Social Security benefits.

That isn’t remotely true, as new data from the Congressional Budget Office demonstrate.
In 2010, payroll taxes covered a little more than a third of
Medicare’s costs. Beneficiary premiums (and some other earmarked
receipts) covered about a seventh. General revenues (which include
borrowing) covered the remainder, slightly more than half of total
Medicare costs.

Last year I published a revised version of my White Paper after a discussion in the Washington Post. Details do mater. But I want to raise another issue.

1. Suppose a couple is married and files jointly. Assume both are over 65. Assume they make jointly $350,000 of income.

2. They pay 3% of the gross for Medicare or $10,500 of their salary.

3. They pay $100 per month plus $150 in addition per month due to their salary. Thus combined they pay $500.00 per month in addition to the Medicare tax. That is $6,000 per year.

4. Combined they pay $16,500 directly for their care. Yes they had paid into Medicare for 40+ years already but we put that aside.

5. They cost the system $11,000 each or a total of $22,000 pa.

6. Net they cost $5,500 which is attributed to a Medicare Fund, which they paid into.

7. Now if they are still working they most likely are still healthy and will probably stay that way thus they really cost nothing and they are penalized $16,500 pa!

This is a strange system but after all it was invented in Washington. And it will only get worse!

The Harvard Crimson announced that the Mayor of Cambridge will try to get the city to limit soft drinks.

They state:

At Monday evening’s City Council meeting, Mayor Henrietta J. Davis
proposed a resolution to investigate the possibility of limiting the
size of sodas and other sugary drinks in local restaurants.

“This
is motivated from a concern about health and children’s health,” said
Davis, who has served as co-chair of the Cambridge Healthy Children Task
Force since 1990.

“All this positive work can only go so far when the environment is filled with two size servings of soda,” Davis said.

The
resolution recommends that the Cambridge Public Health Department
examine whether or not a ban on large servings of soda would help to
reduce obesity. In an emailed statement, the city’s Chief Public Health
Officer Claude-Alix Jacob wrote that the department would have a
decision ready by the fall.

Davis noted the similarities between this resolution and
New York City Mayor Michael Bloomberg’s initiative to limit sodas over
sixteen ounces, an act that has drawn accolades from Alec Baldwin and
criticism from the New York State Restaurant Association, which labeled
the act the “latest in a long list of anti-restaurant initiatives.”

As we have explained with our previous discussion of the Bloomberg Rule, this adds costs but in reality has no effect. One suspects it is a "feel good" approach. Instead of one large soda they get six small ones.

Tuesday, June 19, 2012

I have written extensively on the EHR, electronic health record conundrum, over the past few years but the best description is given in a picture by a patient in this weeks JAMA.

The author states:

No
one was more surprised than the physician himself. The drawing was
unmistakable. It showed the artist—a 7-year-old girl—on the examining
table. Her older sister was seated nearby in a chair, as was her mother,
cradling her baby sister. The doctor sat staring at the computer, his
back to the patient—and everyone else. All were smiling. The picture was
carefully drawn with beautiful colors and details, and you couldn't
miss the message. When he saw the drawing, the physician wrote a caption
for it: “The economic stimulus bill has directed $20 billion to health
care information technology, largely funding electronic medical record
incentives. I wonder how much this technology will really cost?”

It is really worth a view of the picture. I have seen this in various modes:

1. A good friend and superb clinician well over 40 can now be seen asking questions while typing on his screen.

2. A dermatologist friend hired an additional staff person to create her records.

3. A group of residents spend their time looking at screens rather than going to patients.

4. A gerontologist scans his patients from the nurses station, never really looking in to even see if they are alive at a nursing home.

Osler would spin over in his grave. The culture of medicine is being lost. Once we actually looked at the urine and could even identify a disorder by its smell. That is unheard of today. One even uses an electronic stethoscope to record heart beats and use AI technology to seek out beat abnormalities.

Wednesday, June 13, 2012

There is an article in TNR defending Bloomberg's soda ban. As the author states:

The truth is that there’s nothing inherently wrong with paternalistic
government or, in the harsher, feminized shorthand of its detractors,
the “nanny state.” Parents and nannies can be good or bad. No adult
likes to be told how to live his life, but most of us benefit from baby
authoritarianism far more than we’d like to admit. The government
doesn’t want me talking on the phone while I drive? I can’t say I’ve
given that vice up completely, but fear of getting ticketed makes me do
it a lot less than I used to, and I may live longer as a result. The
government wants me eating less salt? I don’t live in New York, but,
when I heard Bloomberg was tightening the noose, I reexamined my
attachment to sodium chloride and found it to be fairly weak. Bloomberg
didn’t want Hitchens to smoke? Hitchens, who died this past December of
throat cancer, went to his grave believing his vices remained none of
Bloomberg’s business. But after being diagnosed in 2010, he conceded
unsentimentally that he had long “been taunting the Reaper into taking a
free scythe in my direction.” If New York City regulations persuade
some of his acolytes to give up cigarettes and thereby avoid his fate,
don’t let’s consider his legacy tarnished.

Now the interesting fact is that Bloomberg is an engineer by training, as are the major heads of the Chinese Government. Now strangely this is like Chinese paternalism, controlling family size. However it is rather un-American, we Americans just don't like being told what to do. You see the vows of poverty, chastity and obedience are truly un-American. But perhaps we are developing the seven deadly sins; sloth, gluttony, envy etc.

4. The sequellae to Type 2 Diabetes can be managed, albeit at a high cost and for an extended period of time.

5. Thus calories are a straight line to massive societal costs.

The question then who pays for this? That is the key point.

1. If we want total freedom then we must insist on allowing the costs to fall where they may. If you do not want to be told what to do then we, the tax payers, will not have any duty to care for you. Like that glutton in Monty Python, one more mint, and kaboom!

2. If we demand society, namely the taxpayer foot the bill for the gluttons, then we have free riders getting a benefit, or the rest of us incurring the liability. This is clearly an unjust situation. Jut Refer to Aristotle Nicomachaen Ethics.

3. However if we demand justice then those gluttons must pay if we allow freedom, namely a non-nanny state. The question then is how to get them to pay? Bloomberg denies this alternative and he wants to stop them.

4. The Bloomberg solution has costs. There will be costs to train, costs to comply, costs to report, and costs for failures, and costs to police. And yet the proposal totally fails to address the real problem, calorie intake. For the true problem, total calories, not soda, must be addressed in some other fashion. Further he focuses on a large soda not on the very product itself. The consumer can disintermediate, get several smaller one. This is a costly and unworkable solution, it will not solve the problem. In fact it is an arrogant solution, and lacking in true recognition of the problem.

5. How to solve the problem. Two ways, both economic. Tax input or tax output and use the funds to pay for the sequallae. It work well on cigarettes, mainly because it was tobacco. But here we have carbs, and their calories. So we can tax all carbs, or tax per excess BMI. Just a simple proposal, since we already have the IRS doing health care compliance, we can have them do weight compliance as well. Thus for example, we can pass a law that requires every person to present themselves at the IRS office for a weigh in once a year. Then for every pound over their maximum we charge then an additional, say, $100 per year. If your maximum weight is say 150 pounds and you weigh 200, you must pay an additional $5000 per year. Imagine, the deficit gone in just one year or less. However one could imagine morbidly obese IRS agents, kindred TSA types, weighing in all of us taxpayers.

Sunday, June 10, 2012

that is a tautology, and a law of nature. The NY Times has a long piece on obesity. It states:

The causes of obesity are everywhere. Societal factors play a big role:
the lack of safe places to play, walk or bike; sedentary jobs; less time
devoted to cooking and more eating out; bigger portion sizes in
packaged and prepared food; and incessant marketing of junk foods that
are high in calories. Sugar-sweetened drinks accounted for at least 20
percent of the increases in weight in the United States between 1977 and
2007, according to one study cited by the institute.

The causes of obesity dear reader are in yourself! Fifty years ago we walked a mile to school, a mile home for lunch, a sandwich, a mile back and then a mile back home at days end. Then I would deliver newspapers on a ten mile route with 123 customers spread all over hell and gone. There was no school lunch, no breakfast, and never had deserts. No money.

Then when running my companies in central Europe, Czech Republic, Greece, Poland, Russia, portions were small and deserts were unheard of.

The worst offender if the Department of Agriculture and its food programs. It is food for the porcine. We should dismantle the program totally. Let kids walk, let them bring their lunch or walk home. Exercise and limited lunches are key. And breakfast at school, just look at the calories of a typical DoA breakfast, it exceeds 1200 cal! That is 70% of the daily maximum intake just there. Then lunch, another 1200. No wonder we have problems, as with so much else, it is the Government!

The Times continues:

The institute says that a major cut in obesity rates will require
multiple strategies on a population-wide scale. This will be even more
challenging than the fight against smoking. But there isn’t any choice
if we want to protect the public’s health, the strength of the economy
and the government budget.

Nonsense. The solution is to just control yourself. Tax weight, tax carbs, and disband the DoA!

Kaiser has had an interview with a former Government bureaucrat who states:

If the whole law goes down, the death rate in the United States will go
up beginning in 2014. Because we know that the number of uninsured
people will not go down, it will go up, and that growth in the number of
uninsured people increases the number of people who die, so it’s pretty
straightforward as far as I can tell. We’ll also have enormous chaos in
the delivery system, but how that will play out exactly is hard to
know.

What is the basis of that statement. People will still be served, no one will be turned away. What will be the cause of this increase. In addition since the law has not yet fully gone into effect, how can there be an increase based on no law if no law was in existence. I may be the Abelard of Health Care but his logic is empty!

He then continues:

As best as anyone can tell, the reaction to the health law has been
founded in an extraordinary amount of misinformation about what’s
actually in it and what it will actually do. And it seems to me there’s
no better way of educating the public about what the law will do and
what effects it will have than just actually proceeding to implement it.
I think when people begin to see exchanges offering a range of
subsidized insurance products, when they begin to see some of the other
things that are happening and not happening as a result of the
legislation, public opinion will catch up.

No perhaps I am not "anyone" but I did read each version and the last final one three times in detail as this blog demonstrates. It is a nightmare! I have repeatedly detailed line by line. And he has the gall to say that:

And it seems to me there’s
no better way of educating the public about what the law will do and
what effects it will have than just actually proceeding to implement it.

We saw that same arrogant attitude from Congress. It is no wonder that people are so opposed. And also if obesity causes Type 2 Diabetes and if Type 2 Diabetes is the major cost element in health care cost explosions then perhaps the man would show by example and take off the weight to reduce the risk.

Today in the NY Times Romer is giving out advice again. But remember it is the very same Romer whose projections on unemployment we have been tracking for almost the past four years, never even close!

I agree that we need more effective fiscal and housing policies. But
neither is likely to happen, at least not before the presidential
election. As a result, the Fed is the only plausible source of immediate
help for the American economy. It was set up as an independent body
precisely so that somebody can do what’s right when politicians can’t or
won’t.

Then she suggests:

After the Fed has pushed interest rates down to zero, its main remaining
tool is communications. It can affect expectations of future growth and
inflation, which can have powerful effects on consumer spending and
business investment today. But to have a big impact, the monetary
actions need to be bold — and pursued with gusto. In an earlier column,
I discussed one of economists’ favorite examples of such a policy:
setting a target for the path of nominal gross domestic product.

If the Fed doesn’t want to do something as drastic as adopting a new
operating procedure, it could at least make any smaller actions it takes
more effective. The previous rounds of quantitative easing
may have done little to improve expectations because their size and
duration were limited in advance. If the Fed does another round, it
should leave the overall size and end date unspecified. Or, better yet,
the ultimate scale and timing could be tied to the goals the Fed wants
to achieve.

Frankly leadership is totally lacking, across the board. It appears that the folks in DC are totally clueless but that perhaps is not totally true. We have shown for four years that the FED has just pumped up the banks and then allowed then to continue to play with money mortgaged on our grandchildren's future. Then we also watch as Fiscal policy runs amok, again total lack of leadership.

Currently the FED is just an observer.A nice place to sit and drink coffee and watch others mess things up. But following the above somewhat vague suggestions based on her track record, please!

Saturday, June 9, 2012

Columbanus was somewhat of a unique individual amongst those at the end of Roman Empire, is such an end can be stretched to the beginning of the seventh century. He stands out for a multitude of reasons that recent authors have noted. Within the past two years three biographies of the wandering Irish monk have been written and they each have certain positive attributes. I review each accordingly. The three books are those by Tristram [[ASIN:1856076865 Columbanus: The earliest voice of Christian Ireland]], Reynolds [[ASIN:0321338898 Columbanus: Light on the Early Middle Ages (Library of World Biography Series)]] and Richards [[ASIN:1845401905 Columbanus]]. I will review each in turn but there is some commonality I shall include in each.

Reynolds has written a splendid work on Columbanus. Of all that I have read his is clearly the best. It is clear, well written, and concise, covers all the points, lacks the risky speculation of others, and fills in the gaps of the world around Columbanus.

Chapter 2 is a summary of what his youth may have been like. There is a great deal available on early Ireland in this time but unlike other areas there were no real cities or centers of humanity, the country was highly disperse and the ruling class was fluid. In addition there was often war like interactions that had been an inherent part of the Irish culture and perhaps that also contributed to the temper we see arising in Columbanus.

Chapter 4 describes his entry into the Monastery. He goes from one at Cleenish on the north end of the Shannon onto Bangor the dominant one at the time. The author makes an excellent reference to the writings of Columbanus at this time on what was to become the Three Chapters controversy. One of the key questions would be; how did the Irish perceive these issues, which were often weighted by Platonic understanding. For example did they have access to Plotinus and they clearly must have been fluent in Greek since many of these writings were in the original Greek. The author has a good discussion on pp 34-35. On p 37 there is a brief discussion on his leaving Bangor and going to Gaul. The details are brief.

In Chapter 5 the author makes a detailed discussion of the "white martyrdom" of leaving Ireland for good. However there is the potential forced return we see later and one may ask how these relate. Chapter 6 is a superb discussion of the Merovingians. The author has done a great job in a few pages of laying out the players, the culture and the issues. However there is the knowing issue of just how well they managed to communicate. This is somewhat discussed out on pp 50-51. Namely the Irish had Latin, as did the Merovingians, but the pronunciation and localisms were significant. It is never clear if Columbanus managed to develop a proficiency in the native Frank language, itself with significant regional variants. On p. 50 when Columbanus enters the land of the Franks one wonders about the communications. Irish was not spoken in the Frank territory nor does it appear that the Irish spoke the Frankish tongue. Latin was a lingua franca but pronunciation and dialects would yet have prevailed. One need look no further than Gregory of Tours and his Latin, a highly clumsy and fragmented Latin, nowhere Ciceronian. Likewise the Latin of Gregory of Rome, the Bishop of Rome, was simple but an amalgam of Roman political style of the late sixth century.

Chapter 7 discusses the battle with the bishops. The author does a superb job in this area. The Irish were egalitarian. They were the first individualists. As such they did not see any reason to be managed by bishops. This would be an ongoing battle for Columbanus. Chapter 8 is a discussion of the miracles. Frankly the discussion of Columbanus and the bears is always delightful but these in many ways is classic for what at the time were people considered saints.

Chapter 9 is quite interesting for it brings Columbanus to the Lombards in and around Milan and to Bobbio his final monastery. Here there are many issues brought up by the author. The Lombards were Arian, namely Christ was from God the Father, not another personhood. Second Columbanus as noted on p 88 he notes "the Irish valued a man's principles more than his position" was in essence the central tenet of individualism. He was not a subject but a person. Further the author states, "Columbanus suggested disobedience if the pope were in error" is noted by the authors as a basis of what one was to see in the Reformation. One could suggest likewise it was also the individualistic nature of the Irish, again one of the only countries NOT occupied by Rome.

There are a few weaknesses, in my opinion.

First, the bibliography is written in a manner which is nearly impossible to read. All references are combined in a single paragraph. Whether this is the author, the publisher, or the editor it is truly a poor and ineffective choice.

Second and this is a question of intent, the book is almost an academic treatise, yet there are no references to sources.

Third and this is a significant issue there are no direct quotes from Columbanus. Many of his works are readily available and hearing his voice would have been useful. Perhaps a new translation would have merit here however.

Fourth, it would have been quite helpful to have contained some of the dialog between Gregory and Columbanus. I understand the problem, namely the Latin is the original, and translations are often poor, but a key point of insight would have been a better understanding of that dialog. Jonas may refer to it but it may very well be a powerful analysis on its own as a window to the new world of the individual versus the subject, the new world view versus the old world view.

As a general note amongst all of the books reviewed, the spelling of names is nowhere consistent. The problem is the multiplicity of sources. This of course is compounded when the spelling is from multiple languages as well.

Why is it useful to understand Columbanus? That in a sense is the underlying theme of each of the three books mentioned. It is especially critical to understand the period between 600-650 AD. As stated by Reynolds in his title, it was the Early Middle Ages, NOT the Dark Ages.

The reasons for better understanding Columbanus and this particular period in history are as follows:

1. Columbanus came from Ireland, and Ireland was never part of the Roman Empire. Thus his world view and that of all the free Irish at the time was not colored by Roman world views. They were never to that point a captive people, they were free and individuals. Thus they belonged to themselves and not to an Empire. Religion was personal.

2. Gregory came from Roman ruling class, a grandson of a Pope. Gregory was effectively at war with Constantinople and the Eastern Church. Gregory did not allegedly understand Greek, Columbanus did, and Gregory was in a sense the last Roman. The Empire was entrenched in Constantinople, and it looked eastward, worrying about Persia. Gregory looked westward, and saw opportunities in the Church in the tribes now living there.

3. Gregory is at odds with Columbanus and the Irish. Gregory was from a world of Groups, one belonged to Rome, one belonged to the Church, and one belonged to the Empire. One was never an individual. The clash was I believe at the heart of the battle between the two. The evidence of that is that Gregory sends an Italian, Augustine, to Canterbury to rule the Church, where logically the Church had a whole nation of educated scholars and devoted believers next door in Ireland. That act was the poke in the eye by Gregory against Columbanus and all Irish and was, in my opinion, the beginning of the battle between England and Ireland which continues to this day.

4. The Arian faith was that of a single God, devoid of the complexities placed and piled atop one another by the early Church Greek Fathers, including the Trinity. The Arians in many ways paralleled the same path seeing humanity in Jesus but not the complexity of Trinitarian Christology. In a sense there is a strong parallel between the Arian faith in a single God and the position of Christ as with the other single God beliefs that included Jesus. The relationship therefore between Columbanus and the Lombards, his work with Theodelinda, the Lombard Queen, and the ability to build his final open monastery in Bobbio was a tribute to his ability to cross the line while maintaining his faith.

5. Columbanus thus represents the advent of the individual, in the context of both the State and the Church. Although respectful of the Bishop of Rome, he showed no humbling before him when it came to discussions of faith. He also showed no bowing before Kings and Queens, he understood how to deal with them. In many ways he was an example of a modern man. There were no national boundaries for Columbanus.

6. In conclusion, I argue that there were no Dark Ages, just a transition from a salve based Empire transitioned into a Middle Ages, which in many ways was a long progression into modern society. The Dark Ages is a term used oftentimes in ignorance. Gibbon talks of the Fall of Rome, was there also a Fall of Carthage? We do not see the Fall of Egypt, Greece, and Persia. Why just Rome? I would argue it was in tune with the British Empire and its world view. Here with Columbanus we have the Birth of the Individual, a single person who can cross lands, tribes, cultures, languages, religions, and talk to a Pope as an equal in thought.

The Hill reports on the plan proposed by two left wing Congress people. It is akin to taking on more ballast when you have split your bottom open. Who in their right mind would ever think of this.

The Hill states:

Sen. Bernie Sanders (I-Vt.) and Rep. Elijah Cummings (D-Md.) on Thursday
proposed a new tax on Wall Street trading that would raise more than
$250 billion over 10 years in order to pay for a new plan to have the
federal government offer dental health insurance coverage to millions of
Americans.

The two members proposed legislation that would
impose a "financial transactions" tax on equity trades that would
collect $2.50 for every $10,000 traded, which would cover stock and bond
trades. That language would reportedly raise an estimated $288 billion
over 10 years, enough to cover the expected $25 billion per year cost of
the new dental plan.

What frankly is basic dental care. Back in the 1950s false teeth were common. Pull out the old ones and glue in the new. Cheap, it worked. Since then we have fluoride, and caries have gone near to zero. Dentists are depending on old folks.

Are we expected to pay for implants? That can be $8,000 per tooth! Are these characters real. Why not keep spending until we are not just broke ... but well Greece, really. I remember when I took a friend from out of the US across the New Hampshire - Vermont border and told him to have passport and visa at the ready. Perhaps that was not a real joke.

Thursday, June 7, 2012

The FED Chairman spoke today regarding the economy. First the drags on the economy we all know:

However, some of the factors that have restrained the recovery
persist. Notably, households and businesses still appear quite cautious
about the economy. For example, according to surveys, households
continue to rate their income prospects as relatively poor and do not
expect economic conditions to improve significantly. Similarly, concerns
about developments in Europe, U.S. fiscal policy, and the strength and
sustainability of the recovery have left some firms hesitant to expand
capacity.

The depressed housing market has also been an important drag on
the recovery. Despite historically low mortgage rates and high levels of
affordability, many prospective homebuyers cannot obtain mortgages, as
lending standards have tightened and the creditworthiness of many
potential borrowers has been impaired. At the same time, a large stock
of vacant houses continues to limit incentives for the construction of
new homes, and a substantial backlog of foreclosures will likely add
further to the supply of vacant homes. However, a few encouraging signs
in housing have appeared recently, including some pickup in sales and
construction, improvements in homebuilder sentiment, and the apparent
stabilization of home prices in some areas.

And he continued:

Even as fiscal policymakers address the urgent issue of fiscal
sustainability, a second objective should be to avoid unnecessarily
impeding the current economic recovery. Indeed, a severe tightening of
fiscal policy at the beginning of next year that is built into current
law--the so-called fiscal cliff--would, if allowed to occur, pose a
significant threat to the recovery.

Moreover, uncertainty about the
resolution of these fiscal issues could itself undermine business and
household confidence.

Fortunately, avoiding the fiscal cliff and
achieving long-term fiscal sustainability are fully compatible and
mutually reinforcing objectives. Preventing a sudden and severe
contraction in fiscal policy will support the transition back to full
employment, which should aid long-term fiscal sustainability. At the
same time, a credible fiscal plan to put the federal budget on a
longer-run sustainable path could help keep longer-term interest rates
low and improve household and business confidence, thereby supporting
improved economic performance today.

A third objective for fiscal policy is to promote a stronger
economy in the medium and long term through the careful design of tax
policies and spending programs.

To the fullest extent possible, federal
tax and spending policies should increase incentives to work and save,
encourage investments in workforce skills, stimulate private capital
formation, promote research and development, and provide necessary
public infrastructure.

Although we cannot expect our economy to grow its
way out of federal budget imbalances without significant adjustment in
fiscal policies, a more productive economy will ease the tradeoffs faced
by fiscal policymakers.

These are well known generalizations. Simply stated we are still in the tank and Congress and the current President must do something but not too much. The incentive comment is a truism. The alternative? Dis-incent this sector? There were no specifics here, no sharp end of the world warnings, and no look to what happens a la Europe.

There must be an adult somewhere who can lay down the warning that will activate the public response.

Now I came from a union family. My father and brother were in the electrical union, my uncle was a senior person in the firefighters union, all in New York. I saw many sides of unions. As The New Republic states:

No, the real underlying story is that unions are losing their
institutional legitimacy in modern America. The problem isn’t that most
people hate unions. The problem for unions is that most people don’t
care about them, or think about them, at all.

In reality, truth be told, many people really do hate unions. I have seen union workers see themselves as set apart, anointed, owed, an worse. They take, do not understand from whom the take, they are often brutes, and are focused on just getting the most from the job, independent of what they do.

There clearly was once a time when unions served a purpose. But today with laws controlling every aspect of employment the need of a union is not only questionable but it has become a veritable drag on our economies.

This is especially true with public unions. I can see this especially in New Jersey where the benefits are extraordinary and the work done is often third rate at best.

The TNR continues:

When union membership peaked in the mid 1950s at about 35 percent, it
was disproportionately weighted to the Northeast, the Midwest, and
California. But that meant that in those regions—the most populous in
the country—either a worker was in a union his/herself, had a family
member in a union, or, at least, had a friend or neighbor in a union.
People, for better or worse, knew what unions did and understood them to be an almost ordinary part of the workings of democratic capitalism.

Most important, they knew, for better or worse, that unions had power.
Sixty years ago, the UAW or the Mineworkers or the Steelworkers, not
only deeply affected crucial sectors of an industrial economy, they also
demanded respect from broader society—demands made manifest in the
“political strikes” they organized, whether legally or not, to protest
the issues of the day.

Yes we had family members, and if truth be told they did not benefit from the union, it was a closed shop world, it kept out competition, it drove shipping from New York, it drove the costs in Manhattan skyrocketing, it complicated everyone's life, and unions did have power. They were and are even more so today a collection of thugs.

The time of unions has come and gone. Yet they are a source of compelled funding of Democrats. Thus they like so many other remnants of the past will continue to be a drag on society.

About Me

Terry has spent most of his career in industry, half in corporate executive positions, and half involved in his start ups. He started on the Faculty and Staff at MIT in 1967 and was there until 1975, and he had returned to MIT from 2005 to 2012 to assist groups of doctoral and post doc students. Terry has focused on a broad set of industries from cable, to satellite, wireless, and even health care software and medical imaging. Terry has published extensively in a broad set of areas as well as having written several books. Terry's view is that of an entrepreneur who has built companies in over twenty countries.
Copyright 2008-2015 Terrence P McGarty all rights reserved.
NOTE: This blog contains personal opinions of the author and is not meant in any manner to provide professional advice, medical advice, financial advice. Reliance on any of the opinions contained herein is done at the risk of the user.

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